The impact of statin therapy on plasma levels of von Willebrand factor antigen

2016 ◽  
Vol 115 (03) ◽  
pp. 520-532 ◽  
Author(s):  
Amirhossein Sahebkar ◽  
Corina Serban ◽  
Sorin Ursoniu ◽  
Dimitri P. Mikhailidis ◽  
Anetta Undas ◽  
...  

SummaryIncreased plasma levels of von Willebrand factor antigen (vWF:Ag) are associated with high risk of coronary artery disease. The effect of statin therapy on vWF:Ag levels remains uncertain. Therefore the aim of this meta-analysis was to evaluate the effect of statin therapy on vWF:Ag Levels. A systematic multiple-database search was carried out to identify randomized controlled trials (RCTs) that investigated the effect of statins on plasma vWF:Ag levels. Random-effect meta-analysis of 21 treatment arms revealed a significant decrease in plasma vWF:Ag levels following statin therapy (SMD: −0.54, 95 %CI: −0.87, −0.21, p=0.001). In subgroup analyses, the greatest effect was observed with simvastatin (SMD: −1.54, 95 %CI: −2.92, −0.17, p=0.028) and pravastatin (SMD: −0.61, 95 %CI: −1.18, −0.04, p=0.035), but not with fluvastatin (SMD: −0.34, 95 %CI: −0.69, 0.02, p=0.065), atorvastatin (SMD: −0.23, 95 %CI: −0.57, 0.11, p=0.179) and rosuvastatin (SMD: −0.20, 95 %CI: −0.71, 0.30, p=0.431). The lowering effect of statins on plasma vWF:Ag levels was greater in the subset of studies lasting ≥ 12 weeks (SMD: −0.70, 95 %CI: −1.19, −0.22, p=0.005) compared with that of studies lasting > 12 weeks (SMD: −0.34, 95 %CI: −0.67, 0.003, p=0.052). Finally, low-intensity statin therapy was not associated with a significant reduction in vWF:Ag levels (SMD: −0.28, 95 %CI: −0.82, 0.27, p=0.320), but a significant effect was observed in high-intensity statin trials (SMD: −0.66, 95 %CI: −1.07, −0.24, p=0.002). This meta-analysis of available RCTs demonstrates a significant reduction in plasma vWF:Ag levels following statin therapy.Note: The review process for this manuscript was fully handled by Christian Weber, Editor in Chief.

1998 ◽  
Vol 92 (3) ◽  
pp. 395-400 ◽  
Author(s):  
D.A.R. Boldy ◽  
P.E. Short ◽  
P. Cowen ◽  
F.G.H. Hill ◽  
D.C. Chambers ◽  
...  

2016 ◽  
Vol 52 (1) ◽  
pp. 91-97 ◽  
Author(s):  
Ahmed Abd El Basset Abo El Ezz ◽  
Maher Ahmed Abd El Hafez ◽  
Doaa Mohamed El Amrousy ◽  
Ghada Abd El Momen Suliman

1992 ◽  
Vol 82 (4) ◽  
pp. 369-376 ◽  
Author(s):  
P. T. Larsson ◽  
N. H. Wallén ◽  
N. Egberg ◽  
P. Hjemdahl

1. The effects of phentolamine (500 μg/min) on platelet aggregability in vivo at rest and during adrenaline infusion were assessed by ex vivo filtragometry and measurements of plasma β-thromboglobulin levels in 10 healthy male subjects. Plasma levels of von Willebrand factor antigen and free fatty acids were also measured. 2. Adrenaline induced marked and expected increases in heart rate and systolic blood pressure and decreased diastolic blood pressure when venous plasma adrenaline levels were elevated from 0.12 ± 0.02 to 2.9 ± 0.3 nmol/l (P < 0.01). 3. Adrenaline caused platelet activation in vivo. Ex vivo filtragometry readings were shortened by 58 ± 9% (P < 0.01), plasma β-thromboglobulin levels increased by 99 ± 44% (P < 0.01) and platelet counts increased by 26 ± 6% (P < 0.01). Plasma levels of von Willebrand factor antigen and free fatty acids increased by 53 ± 5% and 475 ± 113% (both P < 0.01), respectively. 4. Phentolamine enhanced the β-adrenergic vasodilator responses to adrenaline, as both the decrease in diastolic blood pressure and the reflexogenic increase in heart rate were enhanced (both P < 0.01). Marked elevations in plasma noradrenaline levels were found during infusions of phentolamine and adrenaline (P < 0.001). 5. Phentolamine did not alter platelet indices at rest, but abolished adrenaline-induced platelet activation, as filtragometry readings, plasma β-thromboglobulin levels and platelet counts remained at, or below, resting levels. Responses of plasma levels of von Willebrand factor antigen and free fatty acids to adrenaline were not influenced by phentolamine and did not seem to influence platelet responses. 6. Thus, platelet activation by adrenaline in vivo is mediated via α-adrenoceptors, apparently with minor influences of other physiological responses. Circulating and/or locally released catecholamines may activate platelets directly via α-adrenoceptor stimulation during stressful physiological and pathophysiological conditions in humans.


1998 ◽  
Vol 131 (2) ◽  
pp. 151-156 ◽  
Author(s):  
Bernd Jilma ◽  
Thomas Pernerstorfer ◽  
Eva Dirnberger ◽  
Petra Stohlawetz ◽  
Leopold Schmetterer ◽  
...  

Author(s):  
Mohammed Othman Hashim ◽  
Gad Allah Modawe ◽  
Ibrahim Khider Ibrahim

Backgrounds: VonWillebrand disease (VWD) is reportedly the most common inherited bleeding disorder and can also arise as an acquired syndrome (AVWS). These disorders arise due to defects and/or deficiency of the plasma protein von Willebrand factor (VWF)..High plasma vWF concentrations have been reported in patients with various types of cancer, such as prostatic cancer.Metastasization may be associated with activation of haemostatic processes resulting in increased levels of circulating factor VIII-related antigen (FVIIIRAg) (von Willebrand factor antigen). Objective: To evaluate the status of VWF AginSudanese patients with Prostate Cancer attending RICK Methodology: This is a cross-sectional study carried out in Khartoum state at Khartoum oncology (RICK) hospital, during the period from April to June 2018, 45 samples were collected from patients with non-metastatic CA prostate, their ages ranged between 51 to 82 years. The vWF level was measured using Enzyme-linked immunosorbent assay (ELISA). Data were analyzed by the statistical package for social science (SPSS).   Results: Serology for vWF antigen was done for 45 cases of prostate cancer. According to the age, 2(8%) of patients with age 51-66 had a high concentration of VWF while 24(92%) had normal vWF antigen concentration; of those with age 67-82 years, 4(21%) had high vWF antigen and 15(79%) had normal antigen. Conclusion: The study revealedthat more than 80% of Sudanese patients withnon-metastatic prostate cancer have anormal concentration of VWF. Keywords: vWF, Prostate cancer, Age, ELISA


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